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GSE53288
Danio rerio
12 Downloadable Samples
Affymetrix Zebrafish Genome Array (zebrafish)
Description
Microarray data allowed detection of genes that are induced by light in the zebrafish pineal gland
Publication Title
The light-induced transcriptome of the zebrafish pineal gland reveals complex regulation of the circadian clockwork by light.
Sample Metadata Fields
Sex, Specimen part, Treatment, Time
View Samples- Homo sapiens
- 95 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
We examined the microRNAs (miRNAs) expressed in chronic lymphocytic leukemia (CLL) and identified miR-150 as the most abundant, but with leukemia-cell-expression levels that varied among patients. CLL cells that expressed ZAP-70 or that used unmutated IGHV each had a median expression-level of miR-150 that was significantly lower than that of ZAP-70-negative CLL cells or those that used mutated IGHV. In samples stratified for expression of miR-150, CLL cells with low-level miR-150 expressed relatively higher levels of forkhead box P1 (FOXP1) and GRB2-associated binding protein 1 (GAB1), genes with 3 UTRs having evolutionary-conserved binding sites for miR-150. High-level expression of miR-150 could repress expression of these genes, which encode proteins that may enhance B-cell receptor (BCR) signaling, a putative CLL-growth/survival signal. Also, high-level expression of miR-150 levels was a significant independent predictor of longer treatment-free-survival (TFS) or overall survival (OS), whereas an inverse association was observed for high-level expression of GAB1 or FOXP1 for OS. This study demonstrates that expression of miR-150 can influence the relative expression of GAB1 and FOXP1 and the signaling potential of the B-cell receptor (BCR), thereby possibly accounting for the noted association of expression of miR-150 and disease outcome.
Publication Title
miR-150 influences B-cell receptor signaling in chronic lymphocytic leukemia by regulating expression of GAB1 and FOXP1.
Sample Metadata Fields
Specimen part, Disease stage
View Samples- Homo sapiens
- 12 Downloadable Samples
Illumina HiSeq 2500
Description
Using the recently described CD104+/CD44hi antigen combination we demonstrate that tumorigenicity depends on individual cells residing in a hybrid E/M state. Acquisition of this E/M hybrid state is facilitated by the differential expression of EMT- TFs, like Snail accompanied by the expression of adult stem-cell programs. Transition from the highly tumorigenic E/M state to a fully mesenchymal phenotype, achieved by constitutive ectopic expression of Zeb1, is sufficient to drive cells out of the E/M hybrid state into an extreme mesenchymal (xM) state, which is accompanied by a substantial loss of tumorigenicity and a switch from canonical to non-canonical Wnt signaling. Overall design: Performing RNASeq with HMLE (immortalized human mammary epithelial cells) in different EMT stages, either in the E state the hybrid E/M state or the extreme mesenchymal (xM) state as determined by sorting for CD104 and CD44. And performing RNASeq with HMLE cells locked in the xE state by Zeb1KO (xE-SCC-Zeb1KO), from there transferred to the hybrid E/M state by Snail overexpression (E-SCC-Zeb1KOSn) or rescued and transitioned to an xM state with CRISPR resistant Zeb1 wobble mutant (mt) (E-SCC-Zeb1KOSnZmt).
Publication Title
Acquisition of a hybrid E/M state is essential for tumorigenicity of basal breast cancer cells.
Sample Metadata Fields
Specimen part, Subject
View Samples- Homo sapiens
- 16 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Elevated levels of microRNA miR-155 represent a candidate pathogenic factor in chronic B-lymphocytic leukemia (B-CLL). In this study, we present evidence that MYB (v-myb myeloblastosis viral oncogene homolog) is overexpressed in a subset of B-CLL patients. MYB physically associates with the promoter of MIR155 host gene (MIR155HG, also known as BIC, B-cell integration cluster) and stimulates its transcription. This coincides with the hypermethylated histone H3K4 residue and spread hyperacetylation of H3K9 at MIR155HG promoter. Our data provide evidence of oncogenic activities of MYB in B-CLL that include its stimulatory role in MIR155HG transcription.
Publication Title
MYB transcriptionally regulates the miR-155 host gene in chronic lymphocytic leukemia.
Sample Metadata Fields
Specimen part, Disease, Disease stage
View Samples